Heart failure is a debilitating disease in which abnormal function of the heart leads in the direction of inadequate blood flow to fulfill the needs of the tissues and organs of the body. Typically, the heart loses propulsive power because the cardiac muscle loses capacity to stretch and contract. Often, the ventricles do not adequately eject or fill with blood between heartbeats and the valves regulating blood flow become leaky, allowing regurgitation or back-flow of blood. The impairment of arterial circulation deprives vital organs of oxygen and nutrients. Fatigue, weakness and the inability to carry out daily tasks may result. Not all heart failure patients suffer debilitating symptoms immediately. Some may live actively for years. Yet, with few exceptions, the disease is relentlessly progressive. As heart failure progresses, it tends to become increasingly difficult to manage. Even the compensatory responses it triggers in the body may themselves eventually complicate the clinical prognosis. For example, when the heart attempts to compensate for reduced cardiac output, it adds muscle causing the ventricles (particularly the left ventricle) to grow in thickness in an attempt to pump more blood with each heartbeat. This places a still higher demand on the heart's oxygen supply. If the oxygen supply falls short of the growing demand, as it often does, further injury to the heart may result. The additional muscle mass may also stiffen the heart walls to hamper rather than assist in providing cardiac output. A particularly severe form of heart failure is congestive heart failure (CHF) wherein the weak pumping of the heart leads to build-up of fluids in the lungs and other organs and tissues.
Heart failure is often associated with electrical signal conduction defects within the heart. The natural electrical activation system through the heart involves sequential events starting with the sino-atrial (SA) node, and continuing through the atrial conduction pathways of Bachmann's bundle and internodal tracts at the atrial level, followed by the atrio-ventricular (AV) node, the Bundle of His, the right and left bundle branches, with final distribution to the distal myocardial terminals via the Purkinje fiber network. Any of these conduction pathways may potentially be degraded. A common conduction defect arising in connection with CHF is left bundle branch block (LBBB). The left bundle branch forms a broad sheet of conduction fibers along the septal endocardium of the left ventricle and separates into two or three indistinct fascicles. These extend toward the left ventricular apex and innervate both papillary muscle groups. The main bundle branches are nourished by septal perforating arteries. In a healthy heart, electrical signals are conducted more or less simultaneously through the left and right bundles to trigger synchronous contraction of both the septal and postero-lateral walls of the left ventricle. LBBB occurs when conduction of electrical signals through the left bundle branch is delayed or totally blocked, thereby delaying delivery of the electrical signal to the left ventricle and altering the sequence of activation of that ventricle. The impulse starts in the right ventricle (RV) and crosses the septum causing the interventricular septum to depolarize and hence, contract, first. The electrical impulse continues to be conducted to the postero-lateral wall of the left ventricle causing its activation and depolarization but, due to an inability to use the native conduction system, this activation and contraction is delayed. As such, the posterolateral wall of the left ventricle (LV) only starts to contract after the interventricular septum has completed its contraction and is starting to relax. LBBB thus results in an abnormal activation of the left ventricle inducing desynchronized ventricular contraction (i.e. ventricular dyssynchrony) and impairment in cardiac performance.
Degeneration of the electrical conduction system as manifested by LBBB or other conduction defects may come from an acute myocardial infarction but is usually associated with the degeneration as a result of chronic ischemia, left ventricular hypertension, general aging and calcification changes and stretch, especially any form of cardiac myopathy that results in overt CHF. Present treatments are directed towards correcting this electrical correlate by pacing on the left side of the heart and/or pacing on both sides of the left ventricle (lateral-posterior wall and septum) to improve contractile coordination. One particular technique for addressing LBBB is cardiac resynchronization therapy (CRT), which seeks to normalize asynchronous cardiac electrical activation and the resultant asynchronous contractions by delivering synchronized pacing stimulus to both sides of the ventricles using pacemakers or ICDs equipped with biventricular pacing capability, i.e. CRT seeks to reduce or eliminate ventricular dyssynchrony. Ventricular stimulus is synchronized so as to help to improve overall cardiac function. This may have the additional beneficial effect of reducing the susceptibility to life-threatening tachyarrhythmias. With CRT, pacing pulses are delivered directly to the left ventricle in an attempt to ensure that the left ventricular myocardium will contract more uniformly. CRT may also be employed for patients whose nerve conduction pathways are corrupted due to right bundle branch block (RBBB) or due to other problems such as the development of scar tissue within the myocardium following a myocardial infarction. CRT and related therapies are discussed in, for example, U.S. Pat. No. 6,643,546 to Mathis, et al., entitled “Multi-Electrode Apparatus And Method For Treatment Of Congestive Heart Failure”; U.S. Pat. No. 6,628,988 to Kramer, et al., entitled “Apparatus And Method For Reversal Of Myocardial Remodeling With Electrical Stimulation”; and U.S. Pat. No. 6,512,952 to Stahmann, et al., entitled “Method And Apparatus For Maintaining Synchronized Pacing”.
With conventional CRT, an external Doppler-echocardiography system may be used to noninvasively assess cardiac function. It can also be used to assess the effectiveness of any programming changes on overall cardiac function. Then, biventricular pacing control parameters of the pacemaker or ICD are adjusted by a physician using an external programmer in an attempt to synchronize the ventricles and to optimize patient cardiac function. For example, the physician may adjust the interventricular pacing delay, which specifies the time delay between pacing pulses delivered to the right and left ventricles, in an attempt to maximize cardiac output. To assess the effectiveness of any programming change, Doppler-echocardiography, impedance cardiography or some other independent measure of cardiac function is utilized.
However, this evaluation and programming requires an office visit and is therefore a timely and expensive process. It also restricts the evaluation to a resting state, commonly with the patient in a supine position. As such, the system is not necessarily optimized for activity, for the upright position, for other times of day since there may also be a circadian rhythm to cardiac function. Also, heart rate and blood pressure have diurnal or circadian variations. Moreover, when relying on any external hemodynamic monitoring system, the control parameters of the pacemaker or ICD cannot be automatically adjusted to respond to on-going changes in patient cardiac function.
Accordingly, it is desirable to configure the implanted device to automatically and frequently adjust the CRT pacing parameters to reduce the degree of dyssynchrony and improve cardiac output. For the implanted device to adjust CRT pacing parameters effectively, the device should have accurate information regarding the current degree of ventricular dyssynchrony and related cardiac parameters. In particular, the device should have accurate and current information pertaining to each of the following:                the “interventricular delay”—the time delay between contraction of the left and right ventricles;        the “intraventricular electromechanical delay for the RV”—the time interval between electrical activation of the RV and actual contraction of the RV;        the “intraventricular electromechanical delay for the LV”—the time interval between electrical activation of the LV and the actual contraction of the LV;        the “LV systolic interval”—the interval during which the LV contracts;        the “RV systolic interval”—the interval during which the RV contracts;        the “LV diastolic interval”—the interval during which the LV relaxes;        the “RV diastolic interval”—the interval during which the RV relaxes.Of these parameters, the interventricular delay, the systolic intervals, and the diastolic intervals are referred to herein as “mechanical intervals” since these parameters pertain to actual physical contraction of the ventricular chambers. In contrast, the intraventricular delays for the RV and LV are referred to herein as “electromechanical delays” since these parameters pertain to intervals between electrical activation and subsequent mechanical contraction.        
Unfortunately, conventional pacemakers and ICDs are not capable of detecting the aforementioned mechanical and electromechanical parameters. That is, although conventional devices are certainly capable of sensing electrical cardiac signals such as P-waves, R-waves, and T-waves, the devices are not typically capable of sensing actual mechanical contraction of the various chambers of the heart and hence cannot detect the mechanical and electromechanical parameters needed for optimal CRT control. Some state-of-the-art pacemakers have been equipped with acoustic sensors to detect heart sounds representative of at least some mechanical cardiac parameters. See, for example, U.S. patent application Ser. No. 10/346,809 of Min et al., filed Jan. 17, 2003 and entitled “System and Method for Monitoring Cardiac Function via Cardiac Sounds using an Implantable Cardiac Stimulation Device”. Although the techniques of Min et al. are quite useful, the various parameters specific to ventricular dyssynchrony noted above are not detected by those techniques.
In addition, some attempts have been made to use pressure sensors implanted within the ventricles to detect at least some parameters relevant to ventricular dyssynchrony. See, for example, U.S. Published Patent Application 2003/0199934 of Struble et al. entitled “Cardiac Resynchronization with Adaptive A1-A2 and/or V1-V2 Intervals” and U.S. Published Patent Application 2004/0172077 of Chinchoy entitled “Method and Apparatus for Evaluating and Optimizing Ventricular Synchronization”. Struble et al. describes, inter alia, the use of ventricular pressure sensors to determine the time interval between left and right ventricular ejection (as determined based on the upstroke of left and right ventricular pressure measurements.) In particular, left ventricular pressure (LVP) and right ventricular pressure (RVP) measurements are compared to detect the time interval between left and right ventricular ejection. However, reliable detection of LVP is problematic and so it would be desirable to provide alternative techniques for determining the interventricular delay that do not necessarily require an LVP sensor. Also, Struble et al. does not appear to provide techniques for detecting each of the various other ventricular mechanical and electromechanical parameters listed above by exploiting pressure measurements. (Note that Struble et al. also mentions that atrial pressure sensors can be used to determine the time interval between left and right atrial ejection but does not appear to suggest that a combination of atrial and ventricular pressure measurements can be used to detect the interventricular delay or any other parameters specifically pertinent to ventricular dyssynchrony.) The Chinchoy application also describes techniques that exploit both RVP and LVP measurements for use in controlling CRT.
See, also, U.S. Published Patent Application 2006/0009810 of Mann et al. entitled “Method for Detecting, Diagnosing, and Treating Cardiovascular Disease”, which describes, inter alia, various techniques for exploiting left atrial pressure (LAP) measurements to determine various parameters and to evaluate cardiovascular disease. For example, Mann et al. describes techniques for calculating a mechanical atrioventricular (A-V) delay interval based, at least in part, on LAP measurements. The Mann et al. application also describes techniques for evaluating the shapes, relative sizes and intervals between various features of the LAP, such as “a-waves”, “c-waves” and “v-waves”, for use in detecting and diagnosing changes in the severity of various cardiovascular diseases. In one example, an increase in v-wave amplitude along with the merging of the v-wave with the c-wave is deemed to be usually indicative of acute mitral valve regurgitation. However, Mann et al. does not appear to set forth techniques for measuring the interventricular delay as well as the various other ventricular mechanical and electromechanical intervals listed above that are pertinent to ventricular dyssynchrony.
Accordingly, it would be desirable to provide improved techniques for allowing an implantable medical device such as a pacemaker or ICD to directly evaluate ventricular dyssynchrony for use in controlling CRT. In this regard, it is desirable to provide techniques for detecting each of the various parameters listed above that are especially pertinent to ventricular dyssynchrony. It also particularly desirable to provide techniques that permit the interventricular delay to measured without necessarily requiring detection of LVP. It is to these ends that aspects of the invention are directed.